A. History :The name vitamin B6 was suggested by Albert Szent-Györgyi (1934) to designatesubstances, other than thiamine and riboflavin, which cured a dermatitis (acrodynia) in rats. It was, henceforth, also named as adermin or antidermatitis factor. Vitamin B6 group includes 3 compounds : pyridoxine, pyridoxal and pyridoxamine. Pyridoxine was first isolated, in 1938, from yeast and liver. Later, Snell (1942) discovered the other two compounds.
B. Occurrence. The B6 vitamins are widely distributed in nature in plant and animal tissues. They are especially rich in cereals (wheat, rice), peas, turnip greens, brussels sprouts, carrots,potatoes, sweet potatoes, bananas, avocados, watermelons and yeasts. B6 vitamins are also found in egg yolk, salmon, chicken, fish, beaf, pork and liver. Pyridoxine is adequately available in human and cow’s milk. Pyridoxal (PAL) and pyridoxamine (PAM) also occur in nature as their coenzymes, namely, pyridoxal phosphate (PALP) and pyridoxamine phosphate (PAMP), respectively.
C. Structure. All the 3 forms of vitamin B6 are derivatives of pyridine, C5H5N and differ from each other in the nature of substituent at position 4 of the ring. All the 3 forms are readily interconvertible biologically.
D. Properties. Pyridoxine is a white crystalline substance and is soluble in water and alcohol and slightly so in fat solvents. It is sensitive to light and ultraviolet irradition. It is resistant to heat ( i.e., heat-stable) in both acidic and alkaline solutions but its two allies pyridoxal and pyridoxamine are destroyed at high temperatures ( i.e., heat-labile).
E. Metabolism. The various forms of vitamin
B6 serve as growth factors to a number of bacteria. In addition, the 3 forms (pyridoxine, pyridoxal, pyridoxamine) are converted to pyridoxal- 5-phosphate, which acts as a coenzyme in various enzymic reactions involved in amino acid metabolism such as transamination, decarboxylation and racemization and in the metabolism of glycogen and fatty acids. It is also essential in the metabolism of hydroxy amino acids, sulfurcontaining amino acids and also tryptophan.Pyridoxal or its phosphate derivative also possibly acts as a carrier in the active transport of amino acids across cell membranes. Pyridoxine can be converted to either pyridoxal or pyridoxamine but neither of them can be changed to pyridoxine. All these three can be detected in the urine after ingestional though 4-pyridoxic acid is the most important excretion product quantitatively. It is for this reason that when administered in the human body, about 90% of pyridoxine is oxidized to pyridoxic acid and excreted in human urine in this form. B6 vitamins are also essential for the breakdown of kynurenine. When this does not happen, xanthurenic acid appears in the urine. In addition, adequate functioning of the nervous system depends on pyridoxine, deficiency of which leads to seizures and to peripheral neuropathy. Contents Pyridoxal phosphate (PALP) is the coenzyme for both glutamic decarboxylase and γ-aminobutyric acid transaminase; each is essential for normal brain metabolism. It participates in active transport of amino acids across cell membranes, chelates metals, and participates in the synthesis of arachidonic acid from linoleic acid. If it is lacking, glycine metabolism may lead to oxaluria. Normal metabolism of vitamin B6 in higher animals is inhibited by 4-deoxypyridoxine and isonicotinic acid hydrazide (= isoniazid). Isoniazid is noted for its curing properties against tuberculosis.
F. Deficiency. Vitamin B6 deficiency or apyridoxosis in rats leads to the development of acrodynia, a disease of dermatitis on ears, mouth and tail and accompanied by edema and scaliness of these structures. Dogs and chick develop anemia and nervous lesions in apyridoxosis.
In human infants, vitamin B6 deficiency results in convulsions, anemia, dermatitis and gastrointestinal disorders such as nausea and vomiting.
However, this deficiency is rare. Moreover, tryptophan metabolism is also disturbed. In adults, the vitamin B6 deficiency is normally not found because the intestinal bacteria are capable of synthesizing vitamin B6. In B6-deficient anemia, the RBCs are microcytic and hyperchromic. There are increased serum iron concentrations, saturation of iron-binding protein, hemosiderin deposits in bone marrow and liver, and failure of iron utilization for hemoglobin synthesis. Diseases with malabsorption, such as celiac syndrome, may contribute to vitamin B6 deficiency. A syndrome resembling vitamin B6 deficiency, as observed in animals, has also been reported in man during the treatment of tuberculosis with high doses of the drug isoniazid . Only 2-3% of patients receiving conventional doses (2-3mg/kg) of isoniazid developed neuritis ; 40% of patients receiving high doses (20 mg/kg) developed neuropathy. The symptoms were alleviated by the administration of pyridoxine. Thus, 50 mg of pyridoxine per day completely prevented the development of neuritis. It is believed that isoniazid forms a hydrazone complex with pyridoxal, resulting in partial activation of the vitamin. Isoniazid, thus, is a potent antagonist of vitamin B6 .
G. Human requirements. The minimum dietary allowance of vitamin B6 is between 0.2 and
1.2 mg for infants and children and around 2.0 mg for men and women per day. During pregnancy and lactation, the recommended daily dose is 2.5 mg. Pyridoxine antagonists, such as isoniazid used in the treatment of tuberculosis, increase the requirements for pyridoxine as do pregnancy and drugs such as penicillamine, hydralazine and the oral progesterone-estrogen contraceptives.
H. Treatement : Balanced diets usually contain enough pyridoxine so that deficiency is rare. For convulsions due to pyridoxine deficiency, 100 mg of vitamin should be given intramuscularly. Excessive intake may cause sensory neuropathy.
B. Occurrence. The B6 vitamins are widely distributed in nature in plant and animal tissues. They are especially rich in cereals (wheat, rice), peas, turnip greens, brussels sprouts, carrots,potatoes, sweet potatoes, bananas, avocados, watermelons and yeasts. B6 vitamins are also found in egg yolk, salmon, chicken, fish, beaf, pork and liver. Pyridoxine is adequately available in human and cow’s milk. Pyridoxal (PAL) and pyridoxamine (PAM) also occur in nature as their coenzymes, namely, pyridoxal phosphate (PALP) and pyridoxamine phosphate (PAMP), respectively.
C. Structure. All the 3 forms of vitamin B6 are derivatives of pyridine, C5H5N and differ from each other in the nature of substituent at position 4 of the ring. All the 3 forms are readily interconvertible biologically.
D. Properties. Pyridoxine is a white crystalline substance and is soluble in water and alcohol and slightly so in fat solvents. It is sensitive to light and ultraviolet irradition. It is resistant to heat ( i.e., heat-stable) in both acidic and alkaline solutions but its two allies pyridoxal and pyridoxamine are destroyed at high temperatures ( i.e., heat-labile).
E. Metabolism. The various forms of vitamin
B6 serve as growth factors to a number of bacteria. In addition, the 3 forms (pyridoxine, pyridoxal, pyridoxamine) are converted to pyridoxal- 5-phosphate, which acts as a coenzyme in various enzymic reactions involved in amino acid metabolism such as transamination, decarboxylation and racemization and in the metabolism of glycogen and fatty acids. It is also essential in the metabolism of hydroxy amino acids, sulfurcontaining amino acids and also tryptophan.Pyridoxal or its phosphate derivative also possibly acts as a carrier in the active transport of amino acids across cell membranes. Pyridoxine can be converted to either pyridoxal or pyridoxamine but neither of them can be changed to pyridoxine. All these three can be detected in the urine after ingestional though 4-pyridoxic acid is the most important excretion product quantitatively. It is for this reason that when administered in the human body, about 90% of pyridoxine is oxidized to pyridoxic acid and excreted in human urine in this form. B6 vitamins are also essential for the breakdown of kynurenine. When this does not happen, xanthurenic acid appears in the urine. In addition, adequate functioning of the nervous system depends on pyridoxine, deficiency of which leads to seizures and to peripheral neuropathy. Contents Pyridoxal phosphate (PALP) is the coenzyme for both glutamic decarboxylase and γ-aminobutyric acid transaminase; each is essential for normal brain metabolism. It participates in active transport of amino acids across cell membranes, chelates metals, and participates in the synthesis of arachidonic acid from linoleic acid. If it is lacking, glycine metabolism may lead to oxaluria. Normal metabolism of vitamin B6 in higher animals is inhibited by 4-deoxypyridoxine and isonicotinic acid hydrazide (= isoniazid). Isoniazid is noted for its curing properties against tuberculosis.F. Deficiency. Vitamin B6 deficiency or apyridoxosis in rats leads to the development of acrodynia, a disease of dermatitis on ears, mouth and tail and accompanied by edema and scaliness of these structures. Dogs and chick develop anemia and nervous lesions in apyridoxosis.
In human infants, vitamin B6 deficiency results in convulsions, anemia, dermatitis and gastrointestinal disorders such as nausea and vomiting.
However, this deficiency is rare. Moreover, tryptophan metabolism is also disturbed. In adults, the vitamin B6 deficiency is normally not found because the intestinal bacteria are capable of synthesizing vitamin B6. In B6-deficient anemia, the RBCs are microcytic and hyperchromic. There are increased serum iron concentrations, saturation of iron-binding protein, hemosiderin deposits in bone marrow and liver, and failure of iron utilization for hemoglobin synthesis. Diseases with malabsorption, such as celiac syndrome, may contribute to vitamin B6 deficiency. A syndrome resembling vitamin B6 deficiency, as observed in animals, has also been reported in man during the treatment of tuberculosis with high doses of the drug isoniazid . Only 2-3% of patients receiving conventional doses (2-3mg/kg) of isoniazid developed neuritis ; 40% of patients receiving high doses (20 mg/kg) developed neuropathy. The symptoms were alleviated by the administration of pyridoxine. Thus, 50 mg of pyridoxine per day completely prevented the development of neuritis. It is believed that isoniazid forms a hydrazone complex with pyridoxal, resulting in partial activation of the vitamin. Isoniazid, thus, is a potent antagonist of vitamin B6 .G. Human requirements. The minimum dietary allowance of vitamin B6 is between 0.2 and
1.2 mg for infants and children and around 2.0 mg for men and women per day. During pregnancy and lactation, the recommended daily dose is 2.5 mg. Pyridoxine antagonists, such as isoniazid used in the treatment of tuberculosis, increase the requirements for pyridoxine as do pregnancy and drugs such as penicillamine, hydralazine and the oral progesterone-estrogen contraceptives.
H. Treatement : Balanced diets usually contain enough pyridoxine so that deficiency is rare. For convulsions due to pyridoxine deficiency, 100 mg of vitamin should be given intramuscularly. Excessive intake may cause sensory neuropathy.
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